This is the presentation on 'Approach to Cyanosis' for Paediatrics under MBBS curriculum. It focuses of peripheral, central, and differential cyanosis along with their history/examination findings, investigations, and treatment. Good luck!

1. Approach to Cyanosis
Introduction
By Rushali Riah (Roll no. 71)

2. Overview
● Introduction
● Etiology
● History and examination
● Types of cyanosis
● Differential cyanosis
● Investigations
● Treatment

3. What is Cyanosis?
• Cyanosis is derived from the word ‘Cyan' which comes from
‘Kyanos’ the Greek word for BLUE
• Bluish discoloration of skin and mucus membrane when the
concentration of reduced haemoglobin in the capillary bed exceeds
5mg/dl.
• Appears only when an absolute level of haemoglobin is
deoxygenated, so in anemia, the child may be hypoxemic without
showing cyanosis.
• Depends upon total amount of reduced haemoglobin rather than
the ratio of reduced to oxygenated haemoglobin.

4. Mechanism of Cyanosis
• Alveolar Hypoventilation
• Diffusion Impairment
• Ventilation-Perfusion Mismatch
• Right to Left shunting at the intracardiac, great vessels, or
intrapulmonary level.
• Haemoglobinopathy (including Methemoglobinemia) that limits
oxygen transportation.

5. ● Methemoglobinemia is a condition characterized by increased level
of haemoglobin in which iron of heme is oxidized to ferric form
(Fe3+) which is called methemoglobin.
● Methemoglobin is a useless oxygen carrier. So, the level of
deoxygenated hemoglobin significantly elevates causing variable
degree of Cyanosis.

6. Types of Cyanosis
Central
Cyanosis
Peripheral
Cyanosis
Differential
Cyanosis

7. Oxygen dissociation curve
• Sigmoid shape of the oxy-Hb dissociation curve results from the
allosteric interactions of the globin monomers that make up the
haemoglobin tetramer as each one binds O2
• Multiple factors can affect the affinity of Hb for oxygen, thus
causing the curve to shift to the left (increased oxygen affinity)
or to the right (decreased O2 affinity)

9. Factors affecting detection of Cyanosis in
Newborns
1. Haemoglobin Concentration
• Significant oxygen desaturation can be present in anaemic
patients without clinically detectable cyanosis.
• Detected at higher levels of saturation in polycythemic patients
than in anaemic patients.

10. • 2. Fetal Haemoglobin
• Binds more oxygen avidly than adult haemoglobin.
• Oxygen dissociation curve shifts to left. So, for a given level of oxygen
tension (PO2), the oxygen saturation (SO2) is higher in newborns than
older infants or adults.
• Also, for a given level of Oxygen saturation (SO2), the PO2 is lower in
newborns.
• As a result, cyanosis is detected at lower PO2 in newborns. So, in
evaluating a Cyanotic Newborn, both oxygen tension (PO2) and
oxygen saturation (SO2) should be measured to obtain a complete
data.

11. • 3. Skin Pigmentation
• Less apparent in patients with darker complexion.
• Examination of sites like nail beds, tongue and mucus membranes is
more reliable as these are less affected by pigmentation.

12. ETIOLOGY
Leen Saleem Roll no 75

13. Non cardiac
causes
1. Alveoalr hypoventilation
• Asphyxia
• Intraventricular hemorrhage
• Seizure
• Meningitis
• Encephalitis
Central nervous system depression:
• Neonatal myasthenia gravis
• Phrenic nerve injury
• Werdnig-Hoffman disease
Neuromuscular disease:
• Choanal atresia
• Laryngotracheomalacia
• Macroglossia
• Pierre Robin Syndrome
Airway obstruction

14. Non cardiac
causes
2. Ventilation/perfusion mismatch
• Pneumonia
• Aspiration
• Diaphgrahmatic hernia
• Hyaline membrane disease
• Transient tachypnea of newborn
• Atelectasis
Airway disease
• Pneumothorax
• Pleural effusion
• Chylothorax
• Hemothorax
• Thoracic dystropyhy
Extrinsic compression of lungs:

15. Non cardiac
causes
• Methemoglobinemia: congenital
or seconary to toxic exposure
3. Hemoglobinopathy
• Pulmonary edema
• Pulmonary fibrosis
• Congenital lymphangiectasia
4. Diffusion impairment

16. Cardiac
causes
• Tetrallogy of fallot
• Transposition of great vessels
• Total anomalous pulmonary venous return
• Truncus arteriosus
• Tricuspid atresia
Congenital cyanotic heart diseases
• Hypoplastic left heart syndrome
• Coarctation of aorta
• Interrupted aortic arch
• Critival vavular aortic stenosis
Severe heart failure

17. History Taking and
Examination
Ankita Sangwan 76

18. History and
examination
The history and physical examination are
very important in determining the
cause of cyanosis and establishing an
appropriate diagnostic algorithm
It is also possible to differentiate
physiological from pathological with
the history and examination
In taking the history, an attempt should
be made to find out any associated
cardiopulmonary conditions or central
nervous system or any other conditions
that can lead to cyanosis.

19. History of cyanotic patient vary
according to age.
For infants, birth history (Prenatal,
Natal, Post Natal) and age of onset
are important
For older children - family history,
history of trauma, possible ingestion,
choking, medications maybe helpful
Any physical stigmata that maybe
suggested of genetic syndromes
should be noted during examination

20. Drug Intake during pregnancy
Eg. Lithium: Ebstein AnomalyPhenytoin:
Pulmonary Stenosis
Aortic Stenosis
Maternal Diabetic and HTN
TGA, VSD, Hypertrophic Cardiomyopathies
Congenital Intrauterine Infections
Antenatal Fetal echocardiography
Gestational Age
Mode of Delivery and any significant events
during delivery
History
should
mainly focus
on the
following

21. Family history
History of Trauma
Possible ingestion
Choking
Medications

22. Onset of Cyanosis
Early Onset
• Congenital Cyanotic Heart
Diseases,
• Congenital Methoglobineamia
• Genetic Syndromes
• Hyaline Membrane Disease
• Meconium Aspiration
• Oversedation etc
• PROM
Late Onset
• Pulmonary Diseases (eg.
Pneumonia, AV malformation)
• Medications,
• Physiological (eg High Altitude)
• Cold,
• LVF,
• Trauma,
• Shock etc
The onset of cyanosis in the early perinatal period is highly suggestive of a congenital
cause whereas a more recent onset is most likely related to an acquired etiology.

23. Some examples of significant history Suggesting the
diagnosis of certain conditions
Cyanotic Congenital heart conditions
• (Tetralogy of Fallot, Transposition of Great Arteries, Tricuspid atresia, Total
anomalous pulmonary venous connection, Truncus arteriosus)
• Patient may have a history of,
• Previous sibling with congenital heart disease,
• previous dx of congenital heart disease in prenatal period by USG,
• Poor weight gain.
• Tiring easily during play or exercise. Progression to lethargy
• Irritability.
• Prolonged crying
Acquired methemoglobinemia
• Consumption of drug or medication (benzocaine, lidocaine, prilocaine,
• Triptan or furosemide),
• Water contaminated with nitrates,
• Food with high oxidizing agents

24. Some examples of significant history suggesting the
diagnosis of certain conditions
Pneumonia/ Sepsis
• PROM
• Foul smelling liquor
• Maternal Pyrexia
• Maternal GBS
Meconium Aspiration Syndrome
• Post Maturity
• Small for gestational Age
• Placental Dysfunction
• Fetal Distress
• Meconium Stained liquor
Polycythemia
• Small for gestational age
Choanal Atresia
• Bluish discoloration reduce on crying
TTN (transient tachypnea of the
newborn)
• Birth by CS
• Male sex
• Family history of Asthma
• Macrosomia
• Maternal Diabetics
Pneumothoarax
• Aggressive resuscitation
• Meconium Aspiration
Hyaline membrane Disease
• Prematurity
• Maternal Diabetics

25. CLINICAL
EXAMINATION
OF CYANOSIS
Peripheral Cyanosis
Examined under natural light
Sites to look for,
• Tip of nose
• Ear lobe
• Outer aspect of lips
• Tips of fingers and toes
• Palms and soles

26. Central Cyanosis
Examine the patient under natural light
Sites to be looked for:
• Tongue (mainly margin as well as the
undersurface)
• Inner aspect of lips.
• Mucous membrane of gum, palate, cheeks.
• And also look the sites mentioned for peripheral
cyanosis

27. Types of cyanosis
Aayush kumar sah
72

28. Peripheral
cyanosis
It is due to sluggish flow of blood to an
area resulting in greater extraction of
oxygen from normally saturated
arterial blood.
Normal systemic arterial oxygen
saturation

29. Peripheral
cyanosis
Sites:
• Tip of the nose
• Ear lobules
• Outer aspect of lips
• Nailbed of fingers
• Palm and sole

30. Peripheral
cyanosis
Causes:
• Due to local vasoconstriction:
• cold exposure, peripheral vascular
disease
• Due to diminished peripheral blood
flow resulting from reduced cardiac
output
• mitral stenosis, congestive cardiac
failure, shock

31. Central
cyanosis
Due to decreased arterial oxygen saturation
either due to oxygenation defect in lung or
admixture of venous and arterial blood.
Involves highly vascularized tissue through
which blood flow is brisk.
Cardiac output typically is normal, and
patient have warm extremities.
It is evident when oxygen saturation falls
below 90 % from 90 to 95%.

32. Central
cyanosis
Causes:
1. Respiratory disorders:
 Upper airway obstruction
 Respiratory distress syndrome
 Meconium aspiration
 Pneumonia
 PPHN- failure of pulmonary vascular
resistance to fall after birth
 Pulmonary hypoplasia
 Bronchopulmonary dysplasia
 Congenital diaphragmatic hernia
 asthma

33. Central
cyanosis
2. Cardiac disorders
• Cyanotic congenital heart diseases(right to left
shunt)
tetralogy of fallot(TOF)
transoposition of great vessels(TGA)
total anomalous pulmonary venous return
truncus arteriosus
tricuspid atresia
ebstein malformation of the tricuspid valve
left hypoplastic heart
single ventricle
Critical pulmonary atresia

34. Differentiation of cardiac and pulmonary
cyanosis
Cardiac cyanosis Pulmonary cyanosis
Respiration Relatively comfortable at
rest
Tachypnea, distress,
retractions
Crying or effort Cyanosis worsens Cyanosis improves
Auscultation Cardiac murmur Rales, crackles, wheezes
Cardiac silhouette Abnormal shape,
cardiomegaly
Normal obliterated
cardiac margins
ECG Abnormal axis or rhythm Normal
pCO2 Normal or low Usually increased
Response to 100 % o2 Not profound Usually profound

35. Central
cyanosis
3. CNS disorders:
ICH
birth asphyxia
sizures
oversedation
4. Others
polycythemia
methemoglobinemia
metabolic diseases
infection, septicemia
physiological: high altitude- acrocyanosis
”newborn”

36. Central
cyanosis
• Sites:
tongue(mainly margin and under surface)
inner aspect of lips
mucus membrane of gums
soft palate
cheeks

37. Central cyanosis vs peripheral cyanosis
Points Central cyanosis Peripheral cyanosis
Cyanosis Generalised Localised
Affected part Warm Cold
Application of warmth Does not disappear Disappears
Breathing pure oxygen May decrease Cyanosis persists
Tongue Always involved Never involved
Hypoxia Associated Not associated

38. Differential cyanosis
Sandeep Rimal
Roll :72

39. Differential
cyanosis
• Definition : A difference in oxygen
saturation(SaO2) of at least 5 % between the
right arm (preductal) & the legs (postductal)
• Preductal saturation is higher than the
postductal saturation
• So, Upper body pink , lower body blue

40. Causes of
Differential
cyanosis
Critical coarctation of the aorta
Interrrupted aortic arch
PDA with severe pulmonary
hypertension (Eisenmenger syndrome)
Persistent pul. HTN of newborn (PPHN)
with PDA
Severe coarction of Aorta with VSD &
PDA

41. Reverse
differential
cyanosis
• Preductal oxygen saturation is atleast 5%
lower than the postductal saturation
So, legs appear PINK and arms appear BLUE

42. Reverse
differential
cyanosis
• In D-TGA with PDA, Oxygenated blood goes from
pul. Artery to Aorta
• Causes
• D-TGA with PPHN (persistent pul. HTN of newborn)
• D-TGA with interrupted aortic arch
• D-TGA with coarction of aorta
• D-TGA with VSD

43. Intermittent
cyanosis
• Seen in Ebstein’s anomaly

44. INVESTIGATIONS
Apil Sapkota
77

45. PULSE
OXIMETRY
• Standard of care for all infants with
respiratory distress and cyanosis.
• Accurate and reliable method of
monitoring oxygen saturation in infants
noninvasively.
• Normal >=95%
• Considerations- Measurements should not
be performed when the infant is crying or
moving as it reduces the quality of signal
and accuracy of test.

46. Arterial
Blood Gas
Arterial PO2: to confirm central cyanosis :
SaO2 not as good an indicator due
to Increase fetal Hb affinity for O2 (left-shift)
Increase PaCO2: may indicate pulmonary or
CNS disorders, heart failure
Decrease pH: sepsis, circulatory shock, severe
hypoxemia
Methemoglobinemia: Decrease SaO2, normal
PaO2, chocolate-brown blood

47. Hyperoxia
test:
Administer 100 % oxygen for > 10 min
Disease and result (Increase in PaO2)
• Lung disease is more likely than
CHD >150 mmHg
• TGA or severe pulmonary outflow
Obstruction <50 to 60 mmHg
• In lesions with intracardiac mixing
and increased pulmonary blood
flow such as truncus arteriosus >75 to
150mmHg

48. Blood
investigations
CBC
• Increase or decrease WBC : sepsis
• Hematocrit > 65% : polycythemia

49. Chest Xray
• To identify pulmonary causes of
cyanosis: pneumothorax,
pulmonary hypoplasia, diaphragmatic
hernia, pulmonary edema, pleural effusion,
etc.
• Useful in evaluating congenital heart
disease: e.g., cardiomegaly & vascular
congestion: heart failure
• TOF : boot-shaped heart (RVH)
• TGA : egg-on-a-string (anterior/posterior
relationship of great vessels)

50. Pulmonary Oligemia

51. Tetralogy of fallot

52. Transposition of Great Arteries

53. TAPVR

54. ECG
• TOF: Rt axis deviation, wide QRS, rt bundle
branch block
• TGA: Not specific ECG, however RAD can be
seen
• TAPVR: Tall P wave, RAD, ST changes
corresponding to RVH
• Ebstein’s anomaly- Signs of atrial
enlargement, Himalayan P waves i.e p
waves greater than 2.5 mm in height in
leads 2,3 and avF

55. Echocardiogram
• TOF- ventricular septal defect, right
ventricular outflow tract obstruction,
and overriding aorta
• Ebstein’s anomaly- Apical displacement of
the anterior tricuspid valve leaflet
• TGA- pulmonary arteries arising from the
posterior left ventricle, and the aorta rising
anteriorly from the right ventricle.
ventricular septal defect (VSD), patent
ductus arteriosus might also be seen
• TAPVR- Lack of pulmonary venous
connections with the right atrium.
• Hypertrophy of the chambers of right side
of heart
• Right-to-left interatrial connections

56. Treatment of
cyanosis
Manish kumar sah
Roll no:74

57. • Goal-Provide adequate tissue oxygen and co2 removal
• Principles-
• 1.Establish airway
• 2.Ensure oxygenation
• 3.Ensure adequate ventillation
• 4.Correct metabolic abnormalities
• 5.Alleviate the cause of respiratory distress

58. • Monitor airway, breathing, circulation(ABC) with respiratory
compromise, establish an airway and provide supportive
therapy(ego2,machanical ventilation)
• Monitor vital signs
• Establish vascular access for sampling blood and administering
meds(if needed):umbilical vessels convenient for placement of i.v.
and intraarterial catheters
• If sepsis is suspected or another specific cause is not identified
start on broad spectrum antibiotics (eg: ampicillin and
gentamycin)after obtaining a CBC, urinalysis, blood and urine
culture (if possible). Untreated sepsis may lead to pulmonary
disease and ventricular dysfunction

59. • An infant who fails the hyperoxia test and does not have PPHN or
a CXR showing pulmonary disease likely has a CHD that’s ductus
dependent.
• If cardiac disease is suspected,
• Immediately start PGE1 infusion
• Secure a separate i.v. catheter to provide fluids for resuscitation and
• ensure accessibility of intubation equipment should they be required

60. Prostaglandin E1
• For ductal dependent CHD/reduced pulmonary blood flow-Fail
hyperoxia test(An arterial PO2 of <100 torr in the absence of clear
cut lung disease)
• Infusion of prostaglandin E1 at a dose of 0.05-0.1mcg/kg/min i.v.
to maintain patency
• S/E: hypoventilation, apnea, edema and flow grade fever
• Benefits: can be stabilized more easily, allowing for safe transport
to a tertiary center. More time is also available for thorough
diagnostic evaluation and patients can be brought to surgery in a
more stable condition

61. Conclusion
• Identify those that are life threatening.
• Complete maternal and newborn history.
• Perform a thorough physical examination.
• Recognize the common respiratory and cardiac disorders
• Differentiate among various diagnostic entities.
• For ductal dependent lesion, start PGE1 and early referral.